Document Detail


Essential role of leukotriene B4 on Leishmania (Viannia) braziliensis killing by human macrophages.
MedLine Citation:
PMID:  25195516     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Although Leishmania (Viannia) braziliensis is the most prevalent species that cause American tegumentary leishmaniasis (ATL), the immune response against this parasite has been poorly investigated. Upon activation, macrophages produce a series of pro-inflammatory molecules, including the lipid mediator leukotriene B4 (LTB4). LTB4 has been shown to enhance several macrophage functions, but its role in human macrophages is less known. Here, we investigated the role of LTB4 on human monocyte-derived macrophages infected with human isolate of L. (V.) braziliensis (IMG3). It was found that human macrophages produce LTB4 upon infection with Leishmania, which by autocrine or paracrine activation of its high affinity receptor BLT1, potentiates macrophage leishmanicidal activity. This LTB4 effect is mediated by increased secretion of reactive oxygen species (ROS). Moreover, Leishmania infection decreased the expression of BLT1, leading to the speculation that this could represent a parasite escape mechanism to establish a chronic inflammatory infection. Therefore, our data suggest that LTB4 could be used in therapeutic strategies to control Leishmania infection.
Authors:
Camila I Morato; Ildefonso A da Silva; Arissa F Borges; Miriam L Dorta; Milton A P Oliveira; Sonia Jancar; Carlos H Serezani; Fátima Ribeiro-Dias
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-9-4
Journal Detail:
Title:  Microbes and infection / Institut Pasteur     Volume:  -     ISSN:  1769-714X     ISO Abbreviation:  Microbes Infect.     Publication Date:  2014 Sep 
Date Detail:
Created Date:  2014-9-8     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100883508     Medline TA:  Microbes Infect     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2014. Published by Elsevier Masson SAS.
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